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Validated All-in-One™ qPCR Primer for CDK5(NM_004935.3) Search again
Product ID:
HQP000261
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
LIS7, PSSALRE
Gene Description:
cyclin dependent kinase 5
Target Gene Accession:
NM_004935.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- Our data suggest that neurotoxic insults lead to calpain-mediated conversion of p39 to p29, which might contribute to deregulation of Cdk5
- Total cdk5 protein levels are significantly increased in progressive supranuclear palsy brain tissue.
- This suggests a close, stable intermolecular association between cdk5 and phosphorylated tau, consistent with phosphorylation of tau by cdk5 in AD brain.
- CDK5 binds to roscovitine in the ATP-binding pocket
- role in phosphorylation of tau protein
- cdk5 can initiate a major impact on tau pathology progression that probably involves several kinases.
- p25-Cdk5 is responsible for the mitotic-like phosphoepitopes present in neurofibrillary tangles and Cdk5 has a critical role in neurodegenerative mechanisms
- we show that alpha-chimaerin is a Cdk5p35-binding protein; in transfected HeLa cells, Cdk5p35 and alpha-chimaerin displayed an overlapping distribution pattern
- These results suggest that Cdk5/p35 and p25 are novel players in digoxin-triggered prostate cancer cell apoptosis and, therefore, become potential therapeutic targets.
- data suggest that Cyclin-dependent kinase 5 (Cdk5)-Cdk5 activator p35 is required to elicit the maximum GTP-induced secretory response from neutrophils
- an early event in neuronal cell death is p25/Cdk5-mediated retinoblastoma phosphorylation
- These data predict that the ability of cdk5 phosphorylation to protect against htt cleavage, aggregation, and toxicity is compromised in cells expressing toxic fragments of htt.
- role of the CDK5 molecular complex in the genetic etiology of early-onset Alzheimer disease; a yet unknown functional variant in CDK5 or in a nearby gene might lead to increased susceptibility for early-onset Alzheimer disease
- molecular analysis of the CDK5/p25 and CDK2/cyclin A systems
- Mediates exocytosis and decreases beta-amyloid peptide formation in Alzheimer disease.
- nestin is a survival determinant whose action is based upon a novel mode of Cdk5 regulation, affecting the targeting, activity, and turnover of the Cdk5/p35 signaling complex
- phosphorylation of tau at Thr231 and Ser262 by cdk5 plus GSK-3, which inhibits its normal biological activity, is regulated both by its amino terminal inserts and its physical state
- p35 employs pathways distinct from that used by Cdk5 for transport to the nucleus
- phosphorylation of Thr(138) predominantly defines the susceptibility of p35 to calpain-dependent cleavage and that dephosphorylation of this site is a critical determinant of Cdk5-p25-induced cell death associated with neurodegeneration
- Cdk5 kinase supports the proliferation of the medullary thyroid carcinoma cells.
- microtubules play an important role in the control of Cdk5 activation
- Increased expression of Cdk5 was seen in stroke-affected tissue, with about a third showing increased p35 and p25 cleaved fragment. Increased Cdk5-, p-Cdk5- and p35-positive neurons and microvessels occurred in stroke-affected regions.
- Results show that Cdk5, a critical signalling effector of various neurotoxic insults in the brain, is activated by EV71 infection of neuronal cells.
- The Cdk5/DNA damage pathway is dysregulated in Huntington's disease.
- Phosphorylation on a conserved Thr14 can inhibit activities of both the kinases, but phosphorylating another conserved Tyr15, however, can lead to totally opposite inhibition and stimulation consequences in CDK2 and CDK5.
- Thr-138 phosphorylation plays a critical role in the control of the p35 functions in microtubule assembly and neurite outgrowth
- In our analysis, the haplotype tagged by the G allele of SNP rs2069442 was significantly associated with AD (p = 0.05). In conclusion, our study suggests that CDK5 may be associated with AD.
- Cdk5 activation in cells that overexpress cyclin G1 leads to c-Myc phosphorylation on Ser-62, which is responsible for cyclin G1-mediated transcriptional activation of cyclin B1.
- relative resistance to phosphatases might be a common feature of Cdk5 substrates and could contribute to the hyperphosphorylation of CRMP2 and Tau observed in Alzheimer disease
- Cdk5 may cause Golgi fragmentation upon deregulation in Alzheimer's disease
- Cdk5 phosphorylates PIKE-A and stimulates its GTPase activity, which activates nuclear Akt and promotes glioblastoma cell migration and invasion.
- c-Abl and Cdk5 cooperatively regulate maximal activation of p53, resulting in neuronal death in response to oxidative stress by hydrogen peroxide.
- REVIEW. crucial role of Cdk5 as a cell cycle suppressor in normal post-mitotic neurons; Cdk5 exits the nucleus in neurons risk to death in an AD patient's brain. The shift in sub-cellular location is accompanied by cell cycle re-entry and neuronal death.